Endometrial Lesions

Routine histopathology was for long the only readily accessible diagnostic modality, a particular problem in a source tissue which demonstrates dramatic morphological plasticity in response to hormonal stimulation and life cycle changes. The capacity to resolve premalignant lesions in individual patients improved dramatically in the 1990s with the advent of a new molecular toolkit. A key advantage of this approach was the ability to use lesion-specific markers as a unique identifier for premalignant tissue. Specific genetic changes in putative premalignant lesions were confirmed to be carried forward in subsequent carcinomas, thereby confirming direct lineage continuity between premalignant and malignant phases of disease (17,18). For the first time, specific examples of premalignant disease could be confirmed and examined in individual patients.

Contemporary precancer models, which incorporate molecular, cellular, and clinical elements have driven many of the recent developments in the understanding of

Tables 2

Predicted Properties and Level of Evidence for Endometrial Premalignant Lesions

Predicted feature

Associated cancer type

Difference from normal tissue

Differ from carcinoma

Continuous lineage to carcinoma

Can be diagnosed

Increased cancer risk



(type I) Monoclonal

Intermediate PTEN and microsatellite, changes Multiple genetic markers confirm same clone Yes, morphometry or subjective histology




(type II) Initial p53 changes

Intermediate deletional and p53 changes Same p53 mutations

Probably. Must be distinguished from repair Unknown

Serous EICc


(type II) p53 mutations, cytology Not shown

Same p53 mutations

Yes, histology and markers (p53) Yes

^Endometrial intraepithelial neoplasia.

^Endometrial glandular dysplasia.

cSerous endometrial intraepithelial carcinoma.

endometrial carcinogenesis. Predicted biological properties of premalignant endometrial lesions are shown in Table 2, along with the level of existing evidence for candidate endometrial precursors, which have been proposed for types I and II carcinomas. This evidence has been combined in a flow diagram of lesion evolution in Fig. 1, incorporating previously unrecognized endometrial stages, such as "latent precancers" and "endometrial glandular dysplasia," entities whose recognition depends on availability of suitable molecular markers. Caution must be exercised in assigning particular clinical significance to these preclinical lesions, as they might behave quite differently than their clinically diagnosable counterparts.

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